Reversal of Cardiomyopathy by Suppression of Frequent Premature Ventricular Complexes
|ClinicalTrials.gov Identifier: NCT01566344|
Recruitment Status : Unknown
Verified April 2015 by Maastricht University Medical Center.
Recruitment status was: Recruiting
First Posted : March 29, 2012
Last Update Posted : April 10, 2015
|Condition or disease||Intervention/treatment||Phase|
|Heart Diseases Cardiac Arrhythmias Ventricular Premature Complexes Systolic Heart Failure Cardiomyopathies||Other: PVC suppression therapy||Not Applicable|
Heart failure accounts for substantial morbidity and mortality in the western world. In addition, the financial burden associated with the disease is considerable. Prognosis is generally poor and quality of life is significantly reduced. The causes of heart failure are diverse. Identification of the underlying pathophysiological mechanism is essential, because a specific patient tailored therapy may help to improve the clinical status of the individual patient. In addition, some patients may have a potentially reversible cardiomyopathy (CMP). The present study will focus on the role of frequent premature ventricular contractions (PVCs) as a cause of left ventricular (LV) dysfunction. This is a potential reversible CMP generally unknown to the cardiological society.
Frequent ventricular ectopy in patients without structural heart disease is generally thought to be a benign finding with no prognostic significance. Suppression of PVCs with anti-arrhythmic drugs or catheter ablation is therefore usually only considered when PVCs are accompanied by disabling symptoms. However, recent data suggest that frequent monomorphic PVCs (symptomatic or asymptomatic) can cause a form of CMP that may be reversible by suppression of the ectopic focus. Furthermore, the high prevalence of frequent PVCs in patients with heart disease suggests that PVC-induced CMP may be a common phenomenon. Suppression of frequent monomorphic PVCs to improve LV systolic function may therefore emerge as a new and effective treatment strategy for patients with heart failure.
Beta-blockers are safe and effective anti-arrhythmic agents and are considered the first line therapy for suppression of PVCs. Most patients with HF are already taking a beta-blocker as part of standard therapy for their underlying disease. According to international guidelines, other AADs can be used if beta-blockers are ineffective, but they have potential adverse (arrhythmic) side-effects, especially in patients with diminished LV function, and may even be contra-indicated in this patient group. In patients with LV dysfunction and frequent monomorphic PVCs that are refractory to beta-blockers, long-term drug therapy and the potential adverse (arrhythmic) side-effects of AADs can be avoided by using catheter ablation as a first alternative treatment. RFCA is already a frequently applied, widely accepted, safe, effective and potentially curative treatment for symptomatic drug refractory PVCs. It has also been safely and effectively employed in patients with tachycardia-induced CMP and patients with PVC-induced CMP. A high acute success rate of 93% and a very low PVC recurrence rate of 3% have been reported. Although recent available data suggest that elimination of the PVC source by RFCA improves LV systolic function in HF patients, it is still applied in a limited fashion for this indication because the evidence supporting this is weak. The patient series published so far were not controlled and retrospective in nature. We intend to conduct a controlled, randomized, prospective study with careful documentation and long-term follow-up to evaluate the effect of PVC suppression therapy (with RFCA as primary treatment) on cardiac systolic function in patients with CMP and beta-blocker refractory frequent monomorphic PVCs. This could establish suppression of frequent monomorphic PVCs as a potential curative treatment strategy for patients with HF.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||70 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||Single (Outcomes Assessor)|
|Official Title:||Reversal of Cardiomyopathy by Suppression of Frequent Premature Ventricular Complexes - A Prospective Randomized Clinical Trial|
|Study Start Date :||May 2012|
|Estimated Primary Completion Date :||September 2016|
|Estimated Study Completion Date :||December 2016|
|Experimental: Routine heart failure therapy plus PVC suppression therapy||
Other: PVC suppression therapy
Conventional heart failure therapy plus radiofrequency catheter ablation of PVCs as primary treatment and Amiodarone (tablets, loading dose of 600 mg per day for 4 weeks and 200 mg per day afterwards for at least 12 months) as secondary treatment in case of unsuccessful catheter ablation.
|No Intervention: Routine heart failure therapy|
- Change in left ventricular ejection fraction (LVEF) [ Time Frame: Baseline and 6 months ]
- Change in left ventricular end systolic diameter (LVESD) [ Time Frame: Baseline and 6 months ]
- Change in left ventricular end diastolic diameter (LVEDD) [ Time Frame: Baseline and 6 months ]
- Change in left ventricular end systolic volume (LVESV) [ Time Frame: Baseline and 6 months ]
- Change in left ventricular end diastolic volume (LVEDV) [ Time Frame: Baseline and 6 months ]
- Change in New York Heart Association (NYHA) functional class [ Time Frame: Baseline and 6 months ]
- Change in 6 minute walking distance [ Time Frame: Baseline and 6 months ]
- Change in quality of life (QOL) score [ Time Frame: Baseline and 12 months ]
- Change in serum NT-proBNP level [ Time Frame: Baseline and 6 months ]
- Change in premature ventricular complex (PVC) burden [ Time Frame: Baseline and 6 months ]
- Cost-effectiveness: costs from a health service perspective during 12 months follow-up and effectiveness measured as quality adjusted life years (QALY). [ Time Frame: Baseline and 12 months ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01566344
|Contact: Masih Mafi Rad, MDfirstname.lastname@example.org|
|Contact: Yuri Blaauw, MD, PhDemail@example.com|
|Maastricht University Medical Centre||Recruiting|
|Maastricht, Limburg, Netherlands, 6202 AZ|
|Contact: Masih Mafi Rad, MD +31-43-3871613 firstname.lastname@example.org|
|Contact: Yuri Blaauw, MD, PhD +31-43-3877095 email@example.com|
|Sub-Investigator: Masih Mafi Rad, MD|
|Principal Investigator:||Yuri Blaauw, MD, PhD||Maastricht University Medical Centre|
|Principal Investigator:||Harry JGM Crijns, MD, PhD||Maastricht University Medical Centre|